In vitro cleavage of hepatitis B virus C mRNA by 10-23 DNA enzyme

BACKGROUND: 10-23 DNA enzyme is one kind of de-oxyribozymes for RNA cleavage. The inhibition effects of 10-23 DNA enzyme on the expression of the HBV C gene in HepG2. 2. 15 cells were demonstrated previously. The aim of this study was to further explore the cleavage activities of 10-23 DNA enzyme targeting at HBV C gene mRNA in vitro. METHODS: 10-23 DNA enzyme named Drz-HBV-C-9 specific to HBV C gene ORF A1816UG was designed and synthesized. HBV C gene mRNA was obtained by the in vitro transcription method. Cleavage activities of Drz-HBV-C-9 were observed in vitro. Values of kinetic parameters including Km,Kcat and Kcat/Km were calculated accordingly. RESULTS: Under the certain cleavage conditions, Drz-HBV-C-9 could efficiently cleave target mRNA at specific sites in vitro. Cleavage products of 109nt plus 191nt were obtained. The kinetic parameters, Km,Kcat and Kcat/ Km for Drz-HBV-C-9, were 1.4 ×10-9 mol, 1.6 min-1 and 1.1 × 109 mol-1 · min-1, respectively. CONCLUSIONS: 10-23 DNA enzyme targeting at HBV C gene mRNA possesses specific cleavage activities in vitro. This would be a potent antiviral strategy with respect to HBV gene therapy.

Exploitation of host clock gene machinery by hepatitis viruses B and C

Many aspects of cellular physiology display circadian(approximately 24-h)rhythms.Dysfunction of the circadian clock molecular circuitry is associated with human health derangements,including neurodegeneration,increased risk of cancer,cardiovascular diseases and the metabolic syndrome.Viruses triggering hepatitis depend tightly on the host cell synthesis machinery for their own replication,survival and spreading.Recent evidences support a link between the circadian clock circuitry and viruses’biological cycle within host cells.Currently,in vitro models for chronobiological studies of cells infected with viruses need to be implemented.The establishment of such in vitro models would be helpful to better understand the link between the clock gene machinery and viral replication/viral persistence in order to develop specifically targeted therapeutic regimens.Here we review the recent literature dealing with the interplay between hepatitis B and C viruses and clock genes.

Biological impact of hepatitis B virus X-hepatitis C virus core fusion gene on human hepatocytes

AIM: To investigate the biological impact of hepatitis B virus X- hepatitis C virus core (HBV X-HCV C) fusion gene on hepatoma cells. METHODS: The recombinant adenoviruses Ad- XC, Ad-X and Ad-C expressing HBV X-HCV C fusion gene, HBV X gene and HCV C gene were constructed, respectively. Hepatoma cells were infected with different recombinant adenoviruses. MTT, colonyforming experiment, FCM, TUNEL assay were performed to observe the biological impact of the HBV X-HCV C fusion gene on liver cells. RESULTS: MTT showed that the Ad-XC group cells grew faster than the other group cells. Colony-forming experiment showed that the colony-forming rate for the Ad-XC group cells was significantly higher than that for the other group cells. FCM analysis showed that Ad-XC/Ad-X/Ad-C infection enhanced the progression of G1→S phase in the HepG2 cell cycle. The apoptosis index of the Ad-XC, Ad-X, Ad-C group cells was significantly lower than that of the Ad0 and control group cells. Semi-quantitative RT-PCR showed that the expression level of c-myc was the highest in Ad- XC infected cells. Tumor formation was found at the injected site of mice inoculated with Ad-XC-infected LO2 cells, but not in control mice. CONCLUSION: Ad-XC, Ad-X and Ad-C facilitate the proliferation activity of HepG2 cells and inhibit their apoptosis in vitro. The effect of Ad-XC is significantly stronger than that of Ad-X and Ad-C. Up-regulation of c-myc may be one of the mechanisms underlying the synergism of HBV X and HCV C genes on hepatocarcinogenesis in athymic nude mice.

Association of promoter polymorphism of the CD14 C (-159) T endotoxin receptor gene with chronic hepatitis B

AIM: To investigate whether single-nucleotide polymor- phisms in the promoter regions of endotoxin-responsive genes CD14 C (-159) T is associated with chronic hepatitis B. METHODS: We obtained genomic DNA from 80 patients with established diagnosis of chronic hepatitis B and 126 healthy subjects served as a control population. The CD 14 C (-159) T polymorphism was investigated using an allele specific PCR method. RESULTS: Twenty seven percent of chronic hepatitis B patients and 75% of controls were heterozygous for CT genotype. The difference between the chronic hepatitis B and control groups was statistically significant [P < 0.0001; Odds ratio (OR) = 2.887; 95% CI: 1.609-5.178]. Twenty four point six percent of chronic hepatitis B and patients 12.3% of the control group were heterozygous for TT genotype. The difference between groups was not statistically significant (P = 0.256; OR = 0.658; 95% CI: 0.319-1.358). Forty eight point four percent of chronic hepatitis B patients and 12.7% of control were homozy- gote for CC genotype (P < 0.004; OR = 0.416; 95% CI: 0.229-0.755). The frequency of allele C was 61.9% and allele T was 38.1% in hepatitis B patients group. The frequency of allele C was 55.2% and allele T was 44.8% for the control group (P = 0.179; OR = 1.319; 95% CI: 0.881-1.977). CONCLUSION: The TT heterozygous genotype was not a risk factor for chronic hepatitis B. CC homozygote genotype is protective for hepatitis B. Lack of heterozy- gosis of genotype CT is a risk factor for chronic hepatitis B. Alleles C or T were not risk factors for chronic hepatitis B. These findings show the role of a single-nucleotide polymorphism at CD14/-159 on the development ofchronic hepatitis B. Endotoxin susceptibility may play a role in the pathogenesis of chronic hepatitis B.

Nonsense variant of ATP8B1 gene in heterozygosis and benign recurrent intrahepatic cholestasis: A case report and review of literature

BACKGROUND Benign recurrent intrahepatic cholestasis is a genetic disorder with recurrent cholestatic jaundice due to ATP8B1 and ABCB11 gene mutations encoding for hepato-canalicular transporters.Herein,we firstly provide the evidence that a nonsense variant of ATP8B1 gene(c.1558A>T)in heterozygous form is involved in BRIC pathogenesis.CASE SUMMARY A 29-year-old male showed severe jaundice and laboratory tests consistent with intrahepatic cholestasis despite normal gamma-glutamyltranspeptidase.Acute and chronic liver diseases with viral,metabolic and autoimmune etiology were excluded.Normal intra/extra-hepatic bile ducts were demonstrated by magnetic resonance.Liver biopsy showed:Cholestasis in the centrilobular and intermediate zones with bile plugs and intra-hepatocyte pigment,Kupffer’s cell activation/hyperplasia and preserved biliary ducts.Being satisfied benign recurrent intrahepatic cholestasis diagnostic criteria,ATP8B1 and ABCB11 gene analysis was performed.Surprisingly,we found a novel nonsense variant of ATP8B1 gene(c.1558A>T)in heterozygosis.The variant was confirmed by Sanger sequencing following a standard protocol and tested for familial segregation,showing a maternal inheritance.Immunohistochemistry confirmed a significant reduction of mutated gene related protein(familial intrahepatic cholestasis 1).The patient was treated with ursodeoxycholic acid 15 mg/kg per day and colestyramine 8 g daily with total bilirubin decrease and normalization at the 6th and 12th mo.CONCLUSION A genetic abnormality,different from those already known,could be involved in familial intrahepatic cholestatic disorders and/or pro-cholestatic genetic predisposition,thus encouraging further mutation detection in this field.

胃癌组织中c-erb B-2和组织蛋白酶D的表达及其与胃癌生物学行为间的关系

目的 观察癌基因c erbB 2及组织蛋白酶D(Cath D)在胃癌中的表达 ,探讨二者的关系及其与胃癌生物学行为之间的关系。方法 采用免疫组化S P法检测了 10 2例胃癌手术切除标本的c erbB 2及Cath D的表达 ,同时观察了网状纤维分布与c erbB 2和Cath D之间的关系 ,并将检测结果与跟踪随访资料进行了综合分析。结果 10 2例胃癌组织中c erbB 2表达阳性率为 3 8.2 4% (3 9/ 10 2 ) ,与胃癌浸润深度 (P<0 .0 5 )及淋巴结转移 (P<0 .0 5 )密切相关 ;Cath D表达阳性率为 81.3 7% (83 / 10 2 ) ,与胃癌浸润深度 (P<0 .0 5 )、生长方式 (P<0 .0 5 )、淋巴结转移 (P<0 .0 5 )及脉管内有无癌栓 (P<0 .0 5 )有关。生存期分析显示 :Cath D和c erbB 2表达阳性患者预后差 ,5年生存率低于表达阴性患者。结论 c erbB 2及Cath D与胃癌的生长、浸润、转移及预后有密切关系 ,可作为判断胃癌生物学行为和预后的重要指标 ,为临床诊断。

转rolA、B、C基因枳橙快繁技术

通过对转rol基因枳橙B、D、E系及对照的高接植株春梢茎段进行萌芽诱导、增殖及试管苗生根成苗的试验,摸索出适宜枳橙快繁各种培养基配方及培养条件。结果表明,以MS+6-BA1mg/L的培养基适合于芽萌发,以MS+6-BA0.5mg/L+NAA0.05mg/L的培养基适合于芽增殖,生根则以1/2MS+NAA0.5mg/L+0.2%活性炭的组合最佳,转基因各系生根率均在93.3%以上,显著高于对照生根率(66.7%)。快繁苗移栽成活率可达90%,目前生长良好。

Ephrin-B reverse signaling induces expression of wound healing associated genes in IEC-6 intestinal epithelial cells

AIM: Eph receptors and ephrin ligands play a pivotal role in development and tissue maintenance. Since previous data have indicated an involvement of ephrin-B2 in epithelial healing, we investigated the gene expression and downstream signaling pathways induced by ephrin-B mediated cell-cell signaling in intestinal epithelial cells.METHODS: Upon stimulation of ephrin-B pathways in IFC-6 cells with recombinant rat EphB1-Fc, gene expression was analyzed by Affymetrix(R) rat genome 230 high density arrays at different time points. Differentially expressed genes were confirmed by real-time RT-PCR. In addition, MAP kinase pathways and focal adhesion kinase (FAK) activation downstream of ephrin-B were investigated by immunoblotting and fluorescence microscopy.RESULTS: Stimulation of the ephrin-B reverse signaling pathway in IEC-6 cells induces predominant expression of genes known to be involved into wound healing/cell migration, antiapoptotic pathways, host defense and inflammation. Cox-2, c-Fos, Egr-1, Egr-2, and MCP-1 were found among the most significantly regulated genes.Furthermore, we show that the expression of repairrelated genes is also accompanied by activation of the ERK1/2 MAP kinase pathway and FAK, two key regulators of epithelial restitution.CONCLUSION: Stimulation of the ephrin-B reverse signaling pathway induces a phenotype characterized by upregulation of repair-related genes, which may partially be mediated by ERK1/2 pathways.

HBsAg/截短型HCV核心蛋白融合基因对番茄的遗传转化

[目的]本研究旨在探索乙肝病毒表面抗原/截短型HCV核心蛋白融合基因在植物中表达乙肝丙肝双价抗原的可能性,以期为进一步研制植物乙肝丙肝双价口服疫苗打下基础。[方法]应用重组PCR技术将乙肝病毒(HBV)S基因连接在丙肝病毒(HCV)截短型核心蛋白序列的5'端,2者通过柔性肽(Gly4Ser)2序列相连,构建成融合基因BC。将融合基因BC克隆到植物双元表达载体pBin438上,获得pBin438BC,然后用冻融法将其转入根癌农杆菌EHA105中,侵染丽春番茄子叶和下胚轴,经预培养、共培养、脱菌培养、筛选培养、生根培养,提取抗性植株基因组DNA,进行PCR及PCR-Southern检测。[结果]获得了9株抗卡那霉素的番茄植株,5株获得阳性信号。[结论]初步表明目的基因已整合到番茄基因组中。

伊马替尼治疗晚期恶性黑色素瘤C-kit及B-raf基因突变患者的效果研究

目的:探讨伊马替尼对晚期恶性黑色素瘤C-kit及B-raf基因突变者的临床效果。方法:选择2010年1月—2014年1月收治的124例晚期恶性黑色素瘤患者,按照随机数字法分为观察组和对照组,每组各62例。对照组患者给予达卡巴嗪,观察组在对照组治疗的基础上联合应用伊马替尼,对所有患者随访2年,观察2组患者治疗过程中发生的不良反应、疗效及无病生存时间,并比较2组患者1、2年生存率。结果:2组患者化疗不良反应的差异无统计学意义(P>0.05);观察组患者的疾病缓解率为61.29%(38/62),显著高于对照组的22.58%(14/62),差异有统计学意义(P<0.05);观察组患者无病生存时间为(10.2±1.1)个月,显著长于对照组的(5.1±0.3)个月,差异有统计学意义(P<0.05);观察组患者1年及2年生存率均明显高于对照组,差异均有统计学意义(P<0.05)。结论:伊马替尼治疗晚期恶性黑色素瘤C-kit及B-raf基因突变患者,能有效控制疾病进展速度,延长患者生存时间,且不增加治疗过程中的不良反应。

慢性乙型肝炎患者HBV前C区A1896变异和BCP T1762／A1764双变异与临床相关性分析

目的探讨慢性乙型肝炎病毒（HBV）前C区和基本核心启动子（BCP）突变与HBV—DNA载量之间的关系，明确检测突变的意义。方法PCR扩增HBV—DNA前C区序列，进行PCR产物直接测序，测序HBV感染者血清中HBV前C区A1896突变及BCP T1762／A1764双突变例数。结果31例慢性乙型肝炎患者血清HBV—DNA发生nt1896住核苷酸G—A点突变18例；发生nt1762位A—T16例；发生nt1764位G〉A18例；发生nt1762位A—T与1764位G—A双突变16例；1762住A—T1764位G—A双变异和1896位G～A变异的联合变异频率明显高于单个变异。用SPSS16．0软件分析突变与HBV—DNA载量的关系。前C区A1896变异，BCPT1762／A1764变异均与HBV—DNA载量差异无统计学意义。结论HBV—DNA载量仅能反映实时病毒载量，HBV前C区A1896变异和BCPT1762／A1764双变异在各种病毒载量感染者中存在，仅依靠血清学指标及HBV—DNA载量来判断传染性是不够的。检测HBV—DNA前C区A1896变异和BCPT1762／A1764双变异，可辅助判断传染性及制定抗病毒治疗方案。

高脂血症患者APOB/CⅢ/E基因多态性交互作用的研究

目的探讨原发性高脂血症载脂蛋白(Apo)B、CⅢ、E基因中ApoB MspI、ApoB XbaI、ApoB EcorI、ApoCI-II3175、ApoCIII3206、ApoE112/158等7个位点基因多态性间的交互作用。方法采用病例-对照相关性研究策略,选择昆明地区汉族作为研究对象,用基因芯片检测技术,对91例高脂血症患者及76例健康对照者进行ApoB MspI、ApoBXbaI、ApoB EcorI、ApoCⅢ3175、ApoCIII3206、ApoE112/158等6个位点基因多态性进行检测。用比值比(odd ratio,OR)估计相对危险度。用MDR分析多基因相互作用。结果用MDR分析法,对昆明地区汉族高脂血症患者上述6个位点基因型多态性的基因-基因交互作用进行了分析,发现两位点MspI-E112/158、三位点MspI-CIII3206-E112/158和四位点MspI-XbaI-CIII3206-E112/158这三种模型均具有统计学意义(P<0.001),但三位点MspI-CⅢ3206-E112/15模型的交叉验证一致性系数最大(10/10)为最佳模型,该模型包含了位点ApoB MspI、ApoCⅢ3206和ApoE112/158位点,提示这三个基因位点之间可能存在基因-基因交互作用。该模型的Odd Ratio为14.870(95%CI:1.305-169.43)。结论发现昆明地区汉族人群7个高脂血症候选基因位点中,MspI-CIII3206-E112/158三个基因多态性之间可能存在基因-基因交互作用。

颗粒性HBV多CTL表位基因诱导BALB/c小鼠的免疫应答研究

目的:研究含HBV多CTL表位的杂合HBc基因免疫BALB/c小鼠所诱导的免疫应答。方法:构建以HBV多CTL表位取代M IR区基因的杂合HBc基因疫苗(pHBcM ep)并以肌肉注射方式免疫BALB/c小鼠,ELISA、流式细胞术、LDH释放法等分别检测血清特异性抗体与淋巴细胞分泌的IFN-γ水平、CD4+/CD8+T细胞比例变化及特异性CTLs活性等免疫应答指标。结果:颗粒性杂合HBc基因疫苗pHBcM ep免疫BALB/c小鼠诱导明显抗体应答,末次免疫后2周,特异性抗preS2抗体阳性率达100%(12/12),最高效价1∶1 000,同时诱导淋巴细胞分泌IFN-γ能力增强和刺激CTLs活化,其杀伤活性达16 IU30,CD4+/CD8+T细胞比例明显升高,且诱导明显回忆反应。结论:颗粒性HBV多CTL表位基因疫苗pHBcM ep具有良好免疫原性,能迅速诱导高活性体液和细胞免疫应答及回忆反应。

乙型肝炎病毒C区变异与拉米夫定治疗后HBVDNA反弹关系的研究

目的:探讨乙型肝炎病毒(HBV)C区变异及变异位点与拉米夫定抗病毒治疗后HBVDNA反弹的关系。方法:应用PCR-序列分析法,多引物对巢式PCR法,检测10例用拉米夫定治疗的乙型肝炎患者(治疗组),以及10例从未用过抗病毒治疗患者(对照组)的C区的突变位点及HBV基因型。结果:治疗组10例病人中4例检出有C区变异,变异位点分别为:I134V、P164Q、I126L+E142D+P159T及L84I+I88V+I126L+P159A+P164;对照组10例病人中有5例检出有C区变异,变异位点分别为:A83G、A83G+P164QI、126L+P164Q、I126L+P159T;其中I134V、E142D、L84II、88V位点的变异仅出现在拉米夫定治疗后HBVDNA反弹的3例病人中,而且感染的HBV均为C基因型。结论:C区I134V、E142D、L84II、88V位点变异可能与拉米夫定的耐药有关;感染C基因型的病人比B基因型的病人更易出现与拉米夫定耐药相关的C区变异。

青海地区乳腺癌患者B淋巴细胞瘤-2基因C(-938)A多态性与临床生物学指标关系研究

目的探讨青海地区乳腺癌(BC)患者B淋巴细胞瘤-2(Bcl-2)基因C(-938)A多态性(AA、AC、CC基因型)与临床生物学指标的关系。方法选取2014年1月—2015年12月青海大学附属医院乳腺甲状腺外科接受手术治疗的符合纳入标准的BC患者65例为研究对象。术中采集患者BC组织,采用聚合酶链反应-限制性酶切片段长度多态性分析(PCR-RFLP)法检测Bcl-2基因C(-938)A多态性(AA、AC、CC基因型);收集患者临床生物学指标,包括病理类型、肿瘤直径、临床分期、组织学分级、腋窝淋巴结转移数目、雌激素受体(ER)状态、孕激素受体(PR)状态、人表皮生长因子2(HER2)状态、分子分型。采用列联系数χ2检验分析Bcl-2基因C(-938)A多态性与临床生物学指标的关系。结果 65例患者中,AA、CA、CC基因型分别为6、30、29例。由于AA基因型例数少,无法独立分析,故将AA基因型和CC基因型合并分析。Bcl-2基因C(-938)A多态性与病理类型、肿瘤直径、临床分期、组织学分级、腋窝淋巴结转移数目、ER状态、PR状态、HER2状态、分子分型均不存在关联性(P>0.05)。结论青海地区BC患者Bcl-2基因C(-938)A多态性与临床生物学指标病理类型、肿瘤直径、临床分期、组织学分级、腋窝淋巴结转移数目、ER状态、PR状态、HER2状态、分子分型无关。

HBsAg/截短型HCV核心蛋白融合基因植物表达载体的构建及对番茄的遗传转化

探索乙肝病毒表面抗原/截短型HCV核心蛋白融合基因在植物中表达乙肝丙肝双价抗原的可能性.以期为进一步研制植物乙肝丙肝双价口服疫苗打下基础。利用重组PCR技术将乙肝病毒(HBV)S基因连接在丙肝病毒(HCV)截短型核心蛋白序列的5′端,二者通过柔性肽(Gly4Ser)2序列相连,构建成-融合基因BC,测序结果正确。将融合基因BC克降到植物表达载体pBin438上,获得pBin438BC,然后用冻融法将其转入根癌农杆菌EHA105中,采用叶盘法转化番茄。获得了15株抗卡那霉素的番茄植株。对抗性植株进行PCR及Southern检测,8株获得阳性信号,表明目的基因已整合到了番茄基因组中。提取阳性植株的总蛋白.经透析后.将适当浓度蛋白质点在PVDF膜上,用Dot-ELISA方法验证番茄中表达蛋白的活性。结果表明,转基因番茄中有重组蛋白的表达。

Ikaros通过靶向c-KIT抑制B-ALL白血病细胞的增殖

Ikaros是一种重要的造血细胞分化与发育调控因子,其基因结构、蛋白质活性的改变与淋巴细胞白血病的发生密切相关。致癌基因c-KIT与白血病的发生有直接联系,但Ikaros与c-KIT之间的调控关系尚未见报道。本研究报道,在人急性B淋巴细胞白血病(B-acute lymphoblastic leukemia,B-ALL)细胞中,Ikaros可靶向调控c-KIT基因的转录与蛋白质表达。通过在人B-ALL细胞系Nalm6中分别高表达和shRNA干扰Ikaros后,qRT-PCR与Western印迹结果显示,Ikaros可直接抑制c-KIT基因的表达。双荧光素酶报告实验检测Ikaros及其突变体对c-KIT基因的直接靶向作用。结果显示,野生型Ikaros可明显抑制c-KIT的表达,而突变体则不能。进一步利用染色质免疫共沉淀技术(chromatin-immunoprecipitation,Ch IP),检测Ikaros对c-KIT上游启动子序列的结合活力。结果显示,Ikaros蛋白在c-KIT的上游调控区约-500 bp处有明显的结合。Ikaros通过靶向cKIT上游启动子,抑制c-KIT表达,抑制B-ALL细胞的增殖,为临床治疗白血病提供了新思路。

Conservative Evolution of Hepatitis B Virus Precore and Core Gene During Immune Tolerant Phase in Intrafamilial Transmission

Hepatitis B virus(HBV)is characterized with high mutations,which is attributed to the lack of proof-reading of the viral reverse transcriptase and host immune pressure.In this study,31 HBV chronic carriers from 14 families were enrolled to investigate the evolution of the same original HBV sources in different hosts.Sequences of pre-C and C(pre-C/C)genes were analyzed in eight pairs of HBV-infected mothers with longitudinal sera(at an interval of 6.0–7.2 years)and their children(5.5–6.7 years old),and in 15 adults(21–78 years old)from six families with known intrafamilial HBV infection.The pre-C/C sequences had almost no change in eight mothers during 6.0–7.2 years and their children who were in immune tolerant phase.The pre-C/C sequences from the 15 adults of six families,mostly in the immune-clearance phase or the low replicative phase,showed various diversified mutations between individuals from each family.Compared to a reference stain(GQ205441)isolated nearby,the pre-C/C in individuals in immune tolerant phase showed 98.56%–99.52%homology at nucleotide level and 99.5%–100%homology at amino acid level.In contrast,multiple mutations were developed in the immune-clearance phase or the low replicative phase,affecting immune epitopes in core gene and G1896 in pre-C gene.The results indicate that the evolution of new HBV variants is not mainly resulted from the spontaneous error rate of viral reverse transcription,but from the host immune pressure.

Hsa-miR-150过表达诱导弥漫大B淋巴瘤细胞系OCI-Ly10再分化

目的:探究hsa-miR-150过表达诱导弥漫大B淋巴瘤细胞系OCI-Ly10再分化的机制。方法:运用real-time PCR检测hsa-miR-150在永生化CD19+B细胞和OCI-Ly10细胞中的表达,利用Western blotting和免疫荧光细胞化学检测hsa-miR-150靶基因c-myb的表达;通过LipofectamineTM2000脂质体法将含有重组慢病毒质粒的病毒上清转染OCI-Ly10细胞(Ly10-control组和Ly10-miR-150组);对新构建的细胞亚系,通过MTT法检测细胞增殖能力,流式细胞术检测细胞周期及凋亡;运用real-time PCR、免疫荧光细胞化学和Western blotting检测Ly10-control和Ly10-miR-150的B细胞分化相关基因及c-Myb的表达;利用干扰片段干扰OCI-Ly10细胞c-myb表达后,运用real-time PCR和Western blotting检测干扰效率及干扰后转录调节因子BCL6和浆细胞分化开关蛋白PRDM1的表达。结果:(1)CD19+B淋巴细胞的hsa-miR-150表达量明显高于OCI-Ly10细胞(P<0.05);c-Myb在OCI-Ly10细胞中表达较强,而在CD19+B淋巴细胞表达较弱。(2)OCI-Ly10细胞经转染hsa-miR-150后,B细胞分化相关基因的表达都明显发生了变化,B细胞特异性激活蛋白(PAX5)和BCL6表达下调(P<0.05);干扰素调节因子4(IRF4)、PRDM1和X盒结合蛋白1(XBP1)的表达上调(P<0.05);和对照组相比,c-Myb在Ly10-miR-150细胞中表达明显下调(P<0.05)。(3)干扰OCI-Ly10细胞c-myb表达后,BCL6表达明显下调,而PRDM1表达明显上调。结论:(1)hsa-miR-150过表达对OCI-Ly10细胞抑制增殖和诱导凋亡作用非常明显。(2)过表达hsa-miR-150可诱导该瘤细胞向末端B细胞方向分化,作用机制可能与下调其靶基因c-myb的表达有关。